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<title>IARC Scientific Papers</title>
	<link>http://www.iarc.fr/en/feeds/pub_sp/feeds.xml</link>
	<description>This channnel provides the most recent IARC Scientif Papers</description>
	<language>en-us</language>
	<pubDate>Wed, 15 May 2013 20:40:00 GMT</pubDate>
<item>
    <title>Management of colorectal cancer explains differences in 1-year relative survival between France and England for patients diagnosed 1997-2004.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/23392081?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Management of colorectal cancer explains differences in 1-year relative survival between France and England for patients diagnosed 1997-2004.</b></p>
        <p>Br J Cancer. 2013 Mar 5;108(4):775-83</p>
        <p>Authors:  Dejardin O, Rachet B, Morris E, Bouvier V, Jooste V, Haynes R, Coombes EG, Forman D, Jones AP, Bouvier AM, Launoy G</p>
        <p>Abstract<br/>
        BACKGROUND: Few international population-based studies have provided information on potential determinants of international disparities in cancer survival. This population-based study was undertaken to identify the principal differences in disease characteristics and management that accounted for previously observed poorer survival in English compared with French patients with colorectal cancer.<br/>
        METHODS: The study population comprised all cases of colorectal cancer diagnosed between 1997 and 2004 in the areas covered by three population-based cancer registries in France and one in England (N=40 613). To investigate the influence of clinical and treatment variables on survival, we applied multivariable excess hazard modelling based on generalised linear models with Poisson error.<br/>
        RESULTS: Poorer survival for English patients was primarily due to a larger proportion dying within the first year after diagnosis. After controlling for inter-country differences in the use of chemotherapy and surgical resection with curative intent, country of residence was no-longer associated with 1-year survival for advanced colon cancer patients (excess hazard ratio (EHR)=0.99 (0.92-1.01), P=0.095)). Longer term (2-5 years) excess hazards of death for colon and rectal cancer patients did not differ between France and England.<br/>
        CONCLUSION: This study suggests that difference in management close to diagnosis of colon and rectum cancer is related to differences in survival observed between France and England. All efforts (collection and standardisation of additional variables such as co-morbidity) to investigate the reasons for these disparities in management between these two countries, and more generally across Europe, should be encouraged.<br/>
        </p><p>PMID: 23392081 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Dejardin O, Rachet B, Morris E, Bouvier V, Jooste V, Haynes R, Coombes EG, Forman D, Jones AP, Bouvier AM, Launoy G</author>
    <category>Br J Cancer</category>
    <guid isPermaLink="false">PubMed:23392081</guid>
</item>
<item>
    <title>Prediagnostic body fat and risk of death from amyotrophic lateral sclerosis: the EPIC cohort.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/23390184?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Prediagnostic body fat and risk of death from amyotrophic lateral sclerosis: the EPIC cohort.</b></p>
        <p>Neurology. 2013 Feb 26;80(9):829-38</p>
        <p>Authors:  Gallo V, Wark PA, Jenab M, Pearce N, Brayne C, Vermeulen R, Andersen PM, Hallmans G, Kyrozis A, Vanacore N, Vahdaninia M, Grote V, Kaaks R, Mattiello A, Bueno-de-Mesquita HB, Peeters PH, Travis RC, Petersson J, Hansson O, Arriola L, Jimenez-Martin JM, Tjønneland A, Halkjær J, Agnoli C, Sacerdote C, Bonet C, Trichopoulou A, Gavrila D, Overvad K, Weiderpass E, Palli D, Quirós JR, Tumino R, Khaw KT, Wareham N, Barricante-Gurrea A, Fedirko V, Ferrari P, Clavel-Chapelon F, Boutron-Ruault MC, Boeing H, Vigl M, Middleton L, Riboli E, Vineis P</p>
        <p>Abstract<br/>
        OBJECTIVES: The aim of this study was to investigate for the first time the association between body fat and risk of amyotrophic lateral sclerosis (ALS) with an appropriate prospective study design.<br/>
        METHODS: The EPIC (European Prospective Investigation into Cancer and Nutrition) study included 518,108 individuals recruited from the general population across 10 Western European countries. At recruitment, information on lifestyle was collected and anthropometric characteristics were measured. Cox hazard models were fitted to investigate the associations between anthropometric measures and ALS mortality.<br/>
        RESULTS: Two hundred twenty-two ALS deaths (79 men and 143 women) occurred during the follow-up period (mean follow-up = 13 years). There was a statistically significant interaction between categories of body mass index and sex regarding ALS risk (p = 0.009): in men, a significant linear decrease of risk per unit of body mass index was observed (hazard ratio = 0.93, 95% confidence interval 0.86-0.99 per kg/m(2)); among women, the risk was more than 3-fold increased for underweight compared with normal-weight women. Among women, a significant risk reduction increasing the waist/hip ratio was also evident: women in the top quartile had less than half the risk of ALS compared with those in the bottom quartile (hazard ratio = 0.48, 95% confidence interval 0.25-0.93) with a borderline significant p value for trend across quartiles (p = 0.056).<br/>
        CONCLUSION: Increased prediagnostic body fat is associated with a decreased risk of ALS mortality.<br/>
        </p><p>PMID: 23390184 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Gallo V, Wark PA, Jenab M, Pearce N, Brayne C, Vermeulen R, Andersen PM, Hallmans G, Kyrozis A, Vanacore N, Vahdaninia M, Grote V, Kaaks R, Mattiello A, Bueno-de-Mesquita HB, Peeters PH, Travis RC, Petersson J, Hansson O, Arriola L, Jimenez-Martin JM, Tjønneland A, Halkjær J, Agnoli C, Sacerdote C, Bonet C, Trichopoulou A, Gavrila D, Overvad K, Weiderpass E, Palli D, Quirós JR, Tumino R, Khaw KT, Wareham N, Barricante-Gurrea A, Fedirko V, Ferrari P, Clavel-Chapelon F, Boutron-Ruault MC, Boeing H, Vigl M, Middleton L, Riboli E, Vineis P</author>
    <category>Neurology</category>
    <guid isPermaLink="false">PubMed:23390184</guid>
</item>
<item>
    <title>Helicobacter pylori and colonic neoplasms.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/23381070?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Helicobacter pylori and colonic neoplasms.</b></p>
        <p>Am J Gastroenterol. 2013 Feb;108(2):216-7</p>
        <p>Authors:  Plummer M</p>
        <p>Abstract<br/>
        A large cross-sectional survey suggests an association between H. pylori gastritis and colonic neoplasms, but the results should be interpreted with caution.<br/>
        </p><p>PMID: 23381070 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Plummer M</author>
    <category>Am J Gastroenterol</category>
    <guid isPermaLink="false">PubMed:23381070</guid>
</item>
<item>
    <title>Dependence receptor TrkC is a putative colon cancer tumor suppressor.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/23341610?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Dependence receptor TrkC is a putative colon cancer tumor suppressor.</b></p>
        <p>Proc Natl Acad Sci U S A. 2013 Feb 19;110(8):3017-22</p>
        <p>Authors:  Genevois AL, Ichim G, Coissieux MM, Lambert MP, Lavial F, Goldschneider D, Jarrosson-Wuilleme L, Lepinasse F, Gouysse G, Herceg Z, Scoazec JY, Tauszig-Delamasure S, Mehlen P</p>
        <p>Abstract<br/>
        The TrkC neurotrophin receptor belongs to the functional dependence receptor family, members of which share the ability to induce apoptosis in the absence of their ligands. Such a trait has been hypothesized to confer tumor-suppressor activity. Indeed, cells that express these receptors are thought to be dependent on ligand availability for their survival, a mechanism that inhibits uncontrolled tumor cell proliferation and migration. TrkC is a classic tyrosine kinase receptor and therefore generally considered to be a proto-oncogene. We show here that TrkC expression is down-regulated in a large fraction of human colorectal cancers, mainly through promoter methylation. Moreover, we show that TrkC silencing by promoter methylation is a selective advantage for colorectal cell lines to limit tumor cell death. Furthermore, reestablished TrkC expression in colorectal cancer cell lines is associated with tumor cell death and inhibition of in vitro characteristics of cell transformation, as well as in vivo tumor growth. Finally, we provide evidence that a mutation of TrkC detected in a sporadic cancer is a loss-of-proapoptotic function mutation. Together, these data support the conclusion that TrkC is a colorectal cancer tumor suppressor.<br/>
        </p><p>PMID: 23341610 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Genevois AL, Ichim G, Coissieux MM, Lambert MP, Lavial F, Goldschneider D, Jarrosson-Wuilleme L, Lepinasse F, Gouysse G, Herceg Z, Scoazec JY, Tauszig-Delamasure S, Mehlen P</author>
    <category>Proc Natl Acad Sci U S A</category>
    <guid isPermaLink="false">PubMed:23341610</guid>
</item>
<item>
    <title>Population-based study of laparoscopic colorectal cancer surgery 2006-2008.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/23288592?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Population-based study of laparoscopic colorectal cancer surgery 2006-2008.</b></p>
        <p>Br J Surg. 2013 Mar;100(4):553-60</p>
        <p>Authors:  Taylor EF, Thomas JD, Whitehouse LE, Quirke P, Jayne D, Finan PJ, Forman D, Wilkinson JR, Morris EJ</p>
        <p>Abstract<br/>
        BACKGROUND: Clinical guidelines recommend that, where clinically appropriate, laparoscopic tumour resections should be available for patients with colorectal cancer. This study aimed to examine the introduction of laparoscopic surgery in the English National Health Service.<br/>
        METHODS: Data were extracted from the National Cancer Data Repository on all patients who underwent major resection for a primary colorectal cancer diagnosed between 2006 and 2008. Laparoscopic procedures were identified from codes in the Hospital Episode Statistics and National Bowel Cancer Audit Project data in the resource. Trends in the use of laparoscopic surgery and its influence on outcomes were examined.<br/>
        RESULTS: Of 58 135 resections undertaken over the study period, 10 955 (18·8 per cent) were attempted laparoscopically. This increased from 10·0 (95 per cent confidence interval (c.i.) 8·1 to 12·0) per cent in 2006 to 28·4 (25·4 to 31·4) per cent in 2008. Laparoscopic surgery was used less in patients with advanced disease (modified Dukes' stage 'D' versus A: odds ratio (OR) 0·45, 95 per cent c.i. 0·40 to 0·50), rectal tumours (OR 0·71, 0·67 to 0·75), those with more co-morbidity (Charlson score 3 or more versus 0: OR 0·69, 0·58 to 0·82) or presenting as an emergency (OR 0·15, 0·13 to 0·17). A total of 1652 laparoscopic procedures (15·1 per cent) were converted to open surgery. Conversion was more likely in advanced disease (modified Dukes' stage 'D' versus A: OR 1·56, 1·20 to 2·03), rectal tumours (OR 1·29, 1·14 to 1·46) and emergencies (OR 2·06, 1·54 to 2·76). Length of hospital stay (OR 0·65, 0·64 to 0·66), 30-day postoperative mortality (OR 0·55, 0·48 to 0·64) and risk of death within 1 year (hazard ratio 0·60, 0·55 to 0·65) were reduced in the laparoscopic group.<br/>
        CONCLUSION: Laparoscopic surgery was used more frequently in low-risk patients.<br/>
        </p><p>PMID: 23288592 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Taylor EF, Thomas JD, Whitehouse LE, Quirke P, Jayne D, Finan PJ, Forman D, Wilkinson JR, Morris EJ</author>
    <category>Br J Surg</category>
    <guid isPermaLink="false">PubMed:23288592</guid>
</item>
<item>
    <title>Alcohol drinking and endometrial cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) study.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/23273691?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Alcohol drinking and endometrial cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) study.</b></p>
        <p>Ann Epidemiol. 2013 Feb;23(2):93-8</p>
        <p>Authors:  Fedirko V, Jenab M, Rinaldi S, Biessy C, Allen NE, Dossus L, Onland-Moret NC, Schütze M, Tjønneland A, Hansen L, Overvad K, Clavel-Chapelon F, Chabbert-Buffet N, Kaaks R, Lukanova A, Bergmann MM, Boeing H, Trichopoulou A, Oustoglou E, Barbitsioti A, Saieva C, Tagliabue G, Galasso R, Tumino R, Sacerdote C, Peeters PH, Bueno-de-Mesquita HB, Weiderpass E, Gram IT, Sanchez S, Duell EJ, Molina-Montes E, Arriola L, Chirlaque MD, Ardanaz E, Manjer J, Lundin E, Idahl A, Khaw KT, Romaguera-Bosch D, Wark PA, Norat T, Romieu I</p>
        <p>Abstract<br/>
        PURPOSE: Alcohol intake may adversely affect the concentrations of endogenous sex hormones, and thus increase the risk of endometrial cancer. However, epidemiologic studies have provided conflicting results. Therefore, we investigated the association between alcohol intake and endometrial cancer risk a large, multicenter, prospective study.<br/>
        METHODS: From 1992 through 2010, 301,051 women in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort were followed for incident endometrial cancer (n = 1382). Baseline alcohol consumption was assessed by country-specific, validated dietary questionnaires. Information on past alcohol consumption was collected by lifestyle questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated from Cox proportional hazard models.<br/>
        RESULTS: The multivariable HRs (and 95% CIs) compared with light drinkers (0.1-6 g/d) were 1.03 (0.88-1.20) for 0 g of alcohol per day at baseline, 1.01 (0.86-1.17) for 6.1-12 g/d, 1.03 (0.87-1.22) for 12.1-24 g/d, 1.07 (0.87-1.38) for 24.1-36 g/d, and 0.85 (0.61-1.18) for more than 36 g/d (p(trend) = 0.77). No association was observed among former drinkers (OR, 1.28; 95% CI, 0.98-1.68 compared with light drinkers). Null associations were also found between alcohol consumption at age 20 years, lifetime pattern of alcohol drinking, and baseline alcohol intake from specific alcoholic beverages and endometrial cancer risk.<br/>
        CONCLUSIONS: Our findings suggest no association between alcohol intake and endometrial cancer risk.<br/>
        </p><p>PMID: 23273691 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Fedirko V, Jenab M, Rinaldi S, Biessy C, Allen NE, Dossus L, Onland-Moret NC, Schütze M, Tjønneland A, Hansen L, Overvad K, Clavel-Chapelon F, Chabbert-Buffet N, Kaaks R, Lukanova A, Bergmann MM, Boeing H, Trichopoulou A, Oustoglou E, Barbitsioti A, Saieva C, Tagliabue G, Galasso R, Tumino R, Sacerdote C, Peeters PH, Bueno-de-Mesquita HB, Weiderpass E, Gram IT, Sanchez S, Duell EJ, Molina-Montes E, Arriola L, Chirlaque MD, Ardanaz E, Manjer J, Lundin E, Idahl A, Khaw KT, Romaguera-Bosch D, Wark PA, Norat T, Romieu I</author>
    <category>Ann Epidemiol</category>
    <guid isPermaLink="false">PubMed:23273691</guid>
</item>
<item>
    <title>Dietary fiber intake and risk of hormonal receptor-defined breast cancer in the European Prospective Investigation into Cancer and Nutrition study.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/23269820?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Dietary fiber intake and risk of hormonal receptor-defined breast cancer in the European Prospective Investigation into Cancer and Nutrition study.</b></p>
        <p>Am J Clin Nutr. 2013 Feb;97(2):344-53</p>
        <p>Authors:  Ferrari P, Rinaldi S, Jenab M, Lukanova A, Olsen A, Tjønneland A, Overvad K, Clavel-Chapelon F, Fagherazzi G, Touillaud M, Kaaks R, von Rüsten A, Boeing H, Trichopoulou A, Lagiou P, Benetou V, Grioni S, Panico S, Masala G, Tumino R, Polidoro S, Bakker MF, van Gils CH, Ros MM, Bueno-de-Mesquita HB, Krum-Hansen S, Engeset D, Skeie G, Pilar A, Sánchez MJ, Buckland G, Ardanaz E, Chirlaque D, Rodriguez L, Travis R, Key T, Khaw KT, Wareham NJ, Sund M, Lenner P, Slimani N, Norat T, Aune D, Riboli E, Romieu I</p>
        <p>Abstract<br/>
        BACKGROUND: Limited scientific evidence has characterized the association between dietary fiber intake and risk of breast cancer (BC) by menopausal status and hormone receptor expression in tumors.<br/>
        OBJECTIVE: We investigated the relation between total dietary fiber and its main food sources (vegetables, fruit, cereals, and legumes) and BC risk by using data from the European Prospective Investigation into Cancer and Nutrition (EPIC).<br/>
        DESIGN: A total of 11,576 invasive BC cases in 334,849 EPIC women mostly aged 35-70 y at baseline were identified over a median follow-up of 11.5 y. Dietary fiber was estimated from country-specific dietary questionnaires. Multivariable Cox proportional hazards regression models were used to quantify the association between dietary variables and BC risk with energy adjustment by using the residual method. Subgroup analyses were performed by menopausal status and estrogen receptor (ER) and progesterone receptor (PR) expression in tumors.<br/>
        RESULTS: BC risk was inversely associated with intakes of total dietary fiber [hazard ratio comparing fifth quintile to first quintile (HR(Q5-Q1)): 0.95; 95% CI: 0.89, 1.01; P-trend = 0.03] and fiber from vegetables (0.90; 0.84, 0.96; P-trend &lt; 0.01) but not with fiber from fruit, cereals, or legumes. Overall, associations were homogeneous by menopausal status and ER and PR expression in tumors. For vegetable fiber, stronger associations were observed for estrogen receptor-negative and progesterone receptor-negative (HR(Q5-Q1):0.74; 95% CI: 0.59, 0.93; P-trend = 0.01) than for estrogen receptor-positive and progesterone receptor-positive tumors (0.92: 0.81, 1.03; P-trend = 0.05), with P-heterogeneity = 0.09.<br/>
        CONCLUSION: Diets rich in dietary fiber and, particularly, fiber from vegetables may be associated with a small reduction in risk of BC, independently of menopausal status.<br/>
        </p><p>PMID: 23269820 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Ferrari P, Rinaldi S, Jenab M, Lukanova A, Olsen A, Tjønneland A, Overvad K, Clavel-Chapelon F, Fagherazzi G, Touillaud M, Kaaks R, von Rüsten A, Boeing H, Trichopoulou A, Lagiou P, Benetou V, Grioni S, Panico S, Masala G, Tumino R, Polidoro S, Bakker MF, van Gils CH, Ros MM, Bueno-de-Mesquita HB, Krum-Hansen S, Engeset D, Skeie G, Pilar A, Sánchez MJ, Buckland G, Ardanaz E, Chirlaque D, Rodriguez L, Travis R, Key T, Khaw KT, Wareham NJ, Sund M, Lenner P, Slimani N, Norat T, Aune D, Riboli E, Romieu I</author>
    <category>Am J Clin Nutr</category>
    <guid isPermaLink="false">PubMed:23269820</guid>
</item>
<item>
    <title>Smoking water-pipe, chewing nass and prevalence of heart disease: a cross-sectional analysis of baseline data from the Golestan Cohort Study, Iran.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/23257174?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Smoking water-pipe, chewing nass and prevalence of heart disease: a cross-sectional analysis of baseline data from the Golestan Cohort Study, Iran.</b></p>
        <p>Heart. 2013 Feb;99(4):272-8</p>
        <p>Authors:  Islami F, Pourshams A, Vedanthan R, Poustchi H, Kamangar F, Golozar A, Etemadi A, Khademi H, Freedman ND, Merat S, Garg V, Fuster V, Wakefield J, Dawsey SM, Pharoah P, Brennan P, Abnet CC, Malekzadeh R, Boffetta P</p>
        <p>Abstract<br/>
        OBJECTIVE: Water-pipe and smokeless tobacco use have been associated with several adverse health outcomes. However, little information is available on the association between water-pipe use and heart disease (HD). Therefore, we investigated the association of smoking water-pipe and chewing nass (a mixture of tobacco, lime and ash) with prevalent HD.<br/>
        DESIGN: Cross-sectional study.<br/>
        SETTING: Baseline data (collected in 2004-2008) from a prospective population-based study in Golestan Province, Iran.<br/>
        PARTICIPANTS: 50 045 residents of Golestan (40-75 years old; 42.4% men).<br/>
        MAIN OUTCOME MEASURES: ORs and 95% CIs from multivariate logistic regression models for the association of water-pipe and nass use with HD prevalence.<br/>
        RESULTS: A total of 3051 (6.1%) participants reported a history of HD, and 525 (1.1%) and 3726 (7.5%) reported ever water-pipe or nass use, respectively. Heavy water-pipe smoking was significantly associated with HD prevalence (highest level of cumulative use vs never use, OR=3.75; 95% CI 1.52 to 9.22; p for trend=0.04). This association persisted when using different cut-off points, when restricting HD to those taking nitrate compound medications, and among never cigarette smokers. There was no significant association between nass use and HD prevalence (highest category of use vs never use, OR=0.91; 95% CI 0.69 to 1.20).<br/>
        CONCLUSIONS: Our study suggests a significant association between HD and heavy water-pipe smoking. Although the existing evidence suggesting similar biological consequences of water-pipe and cigarette smoking make this association plausible, results of our study were based on a modest number of water-pipe users and need to be replicated in further studies.<br/>
        </p><p>PMID: 23257174 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Islami F, Pourshams A, Vedanthan R, Poustchi H, Kamangar F, Golozar A, Etemadi A, Khademi H, Freedman ND, Merat S, Garg V, Fuster V, Wakefield J, Dawsey SM, Pharoah P, Brennan P, Abnet CC, Malekzadeh R, Boffetta P</author>
    <category>Heart</category>
    <guid isPermaLink="false">PubMed:23257174</guid>
</item>
<item>
    <title>Association between HBX status, aflatoxin-induced R249S TP53 mutation and risk of hepatocellular carcinoma in a case-control study from Thailand.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/23200676?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Association between HBX status, aflatoxin-induced R249S TP53 mutation and risk of hepatocellular carcinoma in a case-control study from Thailand.</b></p>
        <p>Cancer Lett. 2013 Apr 30;331(1):46-51</p>
        <p>Authors:  Ortiz-Cuaran S, Villar S, Gouas D, Ferro G, Plymoth A, Khuhaprema T, Kalalak A, Sangrajrang S, Friesen MD, Groopman JD, Hainaut P</p>
        <p>Abstract<br/>
        Hepatocellular carcinoma (HCC) is associated with hepatitis B virus (HBV) chronicity and dietary exposure to aflatoxin, a mutagen targeting codon 249 of tumor suppressor TP53 (R249S mutation). Based on a case-control in Thailand, we have measured R249S and the status of HBX gene in plasma DNA of 176 cases and 133 referents. Detection of HBX complete sequences was associated with R249S in HCC with no documented prior cirrhosis but not in HCC developing in a context of cirrhosis or in non-cancer chronic liver diseases. Thus, R249S may specifically cooperate with HBX in a pathway to HCC that bypasses cirrhosis.<br/>
        </p><p>PMID: 23200676 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Ortiz-Cuaran S, Villar S, Gouas D, Ferro G, Plymoth A, Khuhaprema T, Kalalak A, Sangrajrang S, Friesen MD, Groopman JD, Hainaut P</author>
    <category>Cancer Lett</category>
    <guid isPermaLink="false">PubMed:23200676</guid>
</item>
<item>
    <title>Smoking and the risk of prostate cancer in the European Prospective Investigation into Cancer and Nutrition.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/23169298?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Smoking and the risk of prostate cancer in the European Prospective Investigation into Cancer and Nutrition.</b></p>
        <p>Br J Cancer. 2013 Feb 19;108(3):708-14</p>
        <p>Authors:  Rohrmann S, Linseisen J, Allen N, Bueno-de-Mesquita HB, Johnsen NF, Tjønneland A, Overvad K, Kaaks R, Teucher B, Boeing H, Pischon T, Lagiou P, Trichopoulou A, Trichopoulos D, Palli D, Krogh V, Tumino R, Ricceri F, Argüelles Suárez MV, Agudo A, Sánchez MJ, Chirlaque MD, Barricarte A, Larrañaga N, Boshuizen H, van Kranen HJ, Stattin P, Johansson M, Bjartell A, Ulmert D, Khaw KT, Wareham NJ, Ferrari P, Romieux I, Gunter MJ, Riboli E, Key TJ</p>
        <p>Abstract<br/>
        BACKGROUND: Smoking is not associated with prostate cancer incidence in most studies, but associations between smoking and fatal prostate cancer have been reported.<br/>
        METHODS: During 1992 and 2000, lifestyle information was assessed via questionnaires and personal interview in a cohort of 145,112 European men. Until 2009, 4623 incident cases of prostate cancer were identified, including 1517 cases of low-grade, 396 cases of high grade, 1516 cases of localised, 808 cases of advanced disease, and 432 fatal cases. Multivariable Cox proportional hazards regression models were used to examine the association of smoking status, smoking intensity, and smoking duration with the risk of incident and fatal prostate cancer.<br/>
        RESULTS: Compared with never smokers, current smokers had a reduced risk of prostate cancer (RR=0.90, 95% CI: 0.83-0.97), which was statistically significant for localised and low-grade disease, but not for advanced or high-grade disease. In contrast, heavy smokers (25+ cigarettes per day) and men who had smoked for a long time (40+ years) had a higher risk of prostate cancer death (RR=1.81, 95% CI: 1.11-2.93; RR=1.38, 95% CI: 1.01-1.87, respectively).<br/>
        CONCLUSION: The observation of an increased prostate cancer mortality among heavy smokers confirms the results of previous prospective studies.<br/>
        </p><p>PMID: 23169298 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Rohrmann S, Linseisen J, Allen N, Bueno-de-Mesquita HB, Johnsen NF, Tjønneland A, Overvad K, Kaaks R, Teucher B, Boeing H, Pischon T, Lagiou P, Trichopoulou A, Trichopoulos D, Palli D, Krogh V, Tumino R, Ricceri F, Argüelles Suárez MV, Agudo A, Sánchez MJ, Chirlaque MD, Barricarte A, Larrañaga N, Boshuizen H, van Kranen HJ, Stattin P, Johansson M, Bjartell A, Ulmert D, Khaw KT, Wareham NJ, Ferrari P, Romieux I, Gunter MJ, Riboli E, Key TJ</author>
    <category>Br J Cancer</category>
    <guid isPermaLink="false">PubMed:23169298</guid>
</item>
<item>
    <title>Shaping chromatin for repair.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/23085398?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Shaping chromatin for repair.</b></p>
        <p>Mutat Res. 2013 Jan-Mar;752(1):45-60</p>
        <p>Authors:  Gospodinov A, Herceg Z</p>
        <p>Abstract<br/>
        To counteract the adverse effects of various DNA lesions, cells have evolved an array of diverse repair pathways to restore DNA structure and to coordinate repair with cell cycle regulation. Chromatin changes are an integral part of the DNA damage response, particularly with regard to the types of repair that involve assembly of large multiprotein complexes such as those involved in double strand break (DSB) repair and nucleotide excision repair (NER). A number of phosphorylation, acetylation, methylation, ubiquitylation and chromatin remodeling events modulate chromatin structure at the lesion site. These changes demarcate chromatin neighboring the lesion, afford accessibility and binding surfaces to repair factors and provide on-the-spot means to coordinate repair and damage signaling. Thus, the hierarchical assembly of repair factors at a double strand break is mostly due to their regulated interactions with posttranslational modifications of histones. A large number of chromatin remodelers are required at different stages of DSB repair and NER. Remodelers physically interact with proteins involved in repair processes, suggesting that chromatin remodeling is a requisite for repair factors to access the damaged site. Together, recent findings define the roles of histone post-translational modifications and chromatin remodeling in the DNA damage response and underscore possible differences in the requirements for these events in relation to the chromatin context.<br/>
        </p><p>PMID: 23085398 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Gospodinov A, Herceg Z</author>
    <category>Mutat Res</category>
    <guid isPermaLink="false">PubMed:23085398</guid>
</item>
<item>
    <title>Proportion cured models applied to 23 cancer sites in Norway.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/22927104?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Proportion cured models applied to 23 cancer sites in Norway.</b></p>
        <p>Int J Cancer. 2013 Apr 1;132(7):1700-10</p>
        <p>Authors:  Cvancarova M, Aagnes B, Fosså SD, Lambert PC, Møller B, Bray F</p>
        <p>Abstract<br/>
        Statistical cure is reached when a group of patients has the same mortality as cancer-free individuals. Cure models predict the cured proportion and the median survival of fatal cases. Cure models have seldom been applied and tested systematically across all major cancer sites. Incidence and follow-up data on 23 cancer sites recorded at the Cancer Registry of Norway 1963-2007 were obtained. Mixture cure models were fitted to obtain trends and up-to-date estimates (based on period approach) assuming cured and uncured groups exist. The model converged for cancers of the mouth and pharynx, oesophagus, stomach, colon, rectum, liver, gallbladder, pancreas, lung and trachea, ovary, kidney, bladder, CNS, non-Hodgkin lymphoma (only for males) and leukemia. The proportion of cured patients increased 1963-2002 for both sexes, with the largest changes (in percent) seen for leukemia (46.4 and 46.7) and CNS (35.9, 42.0), males given first. Median survival time for the uncured cases increased for colon and rectal cancer, and there was a three- fold increase in median survival time for patients with fatal ovarian cancers. Cancers of bladder and CNS had the highest up-to-date proportion cured (in percent), 67.4 and 64.0, respectively, pancreas and liver were amongst the lowest (5.7 and 9.9, respectively). Cure models are useful when monitoring progress in cancer care, but must be applied and interpreted with caution. The absolute estimates of the cure proportion are speculative and should not be calculated where cure is not medically anticipated.<br/>
        </p><p>PMID: 22927104 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Cvancarova M, Aagnes B, Fosså SD, Lambert PC, Møller B, Bray F</author>
    <category>Int J Cancer</category>
    <guid isPermaLink="false">PubMed:22927104</guid>
</item>
<item>
    <title>Prevalence of high-risk human papillomavirus and cervical intraepithelial neoplasias in a previously unscreened population--a pooled analysis from three studies.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/22907663?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Prevalence of high-risk human papillomavirus and cervical intraepithelial neoplasias in a previously unscreened population--a pooled analysis from three studies.</b></p>
        <p>Int J Cancer. 2013 Apr 1;132(7):1693-9</p>
        <p>Authors:  Basu P, Mittal S, Bhaumik S, Mandal SS, Samaddar A, Ray C, Siddiqi M, Biswas J, Sankaranarayanan R</p>
        <p>Abstract<br/>
        Population prevalence of human papillomavirus (HPV) and cervical intraepithelial neoplasias (CIN) is an important indicator to judge the disease burden in the community, to monitor the performance of cervical cancer screening program and to assess the impact of HPV vaccination program. India being a country without any cervical cancer screening program has no published data on the population prevalence of CIN and only a few large community-based studies to report the high-risk HPV prevalence. The objective of our study was to study HPV and CIN prevalence in a previously unscreened population. We pooled together the results of three research studies originally designed to assess the performance of visual inspection after acetic acid application and Hybrid Capture 2 (HC 2). Nearly 60% of the screened women had colposcopy irrespective of their screening test results. The diagnosis and grading of cervical neoplasias were based on histology. The age standardized prevalence of HPV by HC 2 test was 6.0%. Age-adjusted prevalence of CIN1 and CIN2 was 2.3% and 0.5%, respectively. The age-adjusted prevalence of CIN3 was 0.4% and that of invasive cancer was 0.2%. The prevalence of high-risk HPV was relatively low in the population we studied, which is reflected in the low prevalence of high-grade CIN. The prevalence of CIN3 remained constant across age groups due to absence of screening.<br/>
        </p><p>PMID: 22907663 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Basu P, Mittal S, Bhaumik S, Mandal SS, Samaddar A, Ray C, Siddiqi M, Biswas J, Sankaranarayanan R</author>
    <category>Int J Cancer</category>
    <guid isPermaLink="false">PubMed:22907663</guid>
</item>
<item>
    <title>Physical activity and risk of breast cancer overall and by hormone receptor status: the European prospective investigation into cancer and nutrition.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/22903273?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Physical activity and risk of breast cancer overall and by hormone receptor status: the European prospective investigation into cancer and nutrition.</b></p>
        <p>Int J Cancer. 2013 Apr 1;132(7):1667-78</p>
        <p>Authors:  Steindorf K, Ritte R, Eomois PP, Lukanova A, Tjonneland A, Johnsen NF, Overvad K, Østergaard JN, Clavel-Chapelon F, Fournier A, Dossus L, Teucher B, Rohrmann S, Boeing H, Wientzek A, Trichopoulou A, Karapetyan T, Trichopoulos D, Masala G, Berrino F, Mattiello A, Tumino R, Ricceri F, Quirós JR, Travier N, Sánchez MJ, Navarro C, Ardanaz E, Amiano P, Bueno-de-Mesquita HB, van Duijnhoven F, Monninkhof E, May AM, Khaw KT, Wareham N, Key TJ, Travis RC, Borch KB, Sund M, Andersson A, Fedirko V, Rinaldi S, Romieu I, Wahrendorf J, Riboli E, Kaaks R</p>
        <p>Abstract<br/>
        Physical activity is associated with reduced risks of invasive breast cancer. However, whether this holds true for breast cancer subtypes defined by the estrogen receptor (ER) and the progesterone receptor (PR) status is controversial. The study included 257,805 women from the multinational EPIC-cohort study with detailed information on occupational, recreational and household physical activity and important cofactors assessed at baseline. During 11.6 years of median follow-up, 8,034 incident invasive breast cancer cases were identified. Data on ER, PR and combined ER/PR expression were available for 6,007 (67.6%), 4,814 (54.2%) and 4,798 (53.9%) cases, respectively. Adjusted hazard ratios (HR) were estimated by proportional hazards models. Breast cancer risk was inversely associated with moderate and high levels of total physical activity (HR = 0.92, 95% confidence interval (CI): 0.86-0.99, HR = 0.87, 95%-CI: 0.79-0.97, respectively; p-trend = 0.002), compared to the lowest quartile. Among women diagnosed with breast cancer after age 50, the largest risk reduction was found with highest activity (HR = 0.86, 95%-CI: 0.77-0.97), whereas for cancers diagnosed before age 50 strongest associations were found for moderate total physical activity (HR = 0.78, 95%-CI: 0.64-0.94). Analyses by hormone receptor status suggested differential associations for total physical activity (p-heterogeneity = 0.04), with a somewhat stronger inverse relationship for ER+/PR+ breast tumors, primarily driven by PR+ tumors (p-heterogeneity &lt; 0.01). Household physical activity was inversely associated with ER-/PR- tumors. The results of this largest prospective study on the protective effects of physical activity indicate that moderate and high physical activity are associated with modest decreased breast cancer risk. Heterogeneities by receptor status indicate hormone-related mechanisms.<br/>
        </p><p>PMID: 22903273 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Steindorf K, Ritte R, Eomois PP, Lukanova A, Tjonneland A, Johnsen NF, Overvad K, Østergaard JN, Clavel-Chapelon F, Fournier A, Dossus L, Teucher B, Rohrmann S, Boeing H, Wientzek A, Trichopoulou A, Karapetyan T, Trichopoulos D, Masala G, Berrino F, Mattiello A, Tumino R, Ricceri F, Quirós JR, Travier N, Sánchez MJ, Navarro C, Ardanaz E, Amiano P, Bueno-de-Mesquita HB, van Duijnhoven F, Monninkhof E, May AM, Khaw KT, Wareham N, Key TJ, Travis RC, Borch KB, Sund M, Andersson A, Fedirko V, Rinaldi S, Romieu I, Wahrendorf J, Riboli E, Kaaks R</author>
    <category>Int J Cancer</category>
    <guid isPermaLink="false">PubMed:22903273</guid>
</item>
<item>
    <title>Fish consumption and subsequent change in body weight in European women and men.</title>
    <link>http://www.ncbi.nlm.nih.gov/pubmed/22716915?dopt=Abstract</link>    
    <description>
	<![CDATA[
        <p><b>Fish consumption and subsequent change in body weight in European women and men.</b></p>
        <p>Br J Nutr. 2013 Jan 28;109(2):353-62</p>
        <p>Authors:  Jakobsen MU, Dethlefsen C, Due KM, May AM, Romaguera D, Vergnaud AC, Norat T, Sørensen TI, Halkjær J, Tjønneland A, Boutron-Ruault MC, Clavel-Chapelon F, Fagherazzi G, Teucher B, Kühn T, Bergmann MM, Boeing H, Naska A, Orfanos P, Trichopoulou A, Palli D, Santucci De Magistris M, Sieri S, Bueno-de-Mesquita HB, van der A DL, Engeset D, Hjartåker A, Rodríguez L, Agudo A, Molina-Montes E, Huerta JM, Barricarte A, Amiano P, Manjer J, Wirfält E, Hallmans G, Johansson I, Khaw KT, Wareham NJ, Key TJ, Chajès V, Slimani N, Riboli E, Peeters PH, Overvad K</p>
        <p>Abstract<br/>
        Fish consumption is the major dietary source of EPA and DHA, which according to rodent experiments may reduce body fat mass and prevent obesity. Only a few human studies have investigated the association between fish consumption and body-weight gain. We investigated the association between fish consumption and subsequent change in body weight. Women and men (n 344,757) participating in the European Prospective Investigation into Cancer and Nutrition were followed for a median of 5.0 years. Linear and logistic regression were used to investigate the associations between fish consumption and subsequent change in body weight. Among women, the annual weight change was 5.70 (95 % CI 4.35, 7.06), 2.23 (95 % CI 0.16, 4.31) and 11.12 (95 % CI 8.17, 14.08) g/10 g higher total, lean and fatty fish consumption per d, respectively. The OR of becoming overweight in 5 years among women who were normal weight at enrolment was 1.02 (95 % CI 1.01, 1.02), 1.01 (95 % CI 1.00, 1.02) and 1.02 (95 % CI 1.01, 1.04) g/10 g higher total, lean and fatty consumption per d, respectively. Among men, fish consumption was not statistically significantly associated with weight change. Adjustment for potential over- or underestimation of fish consumption did not systematically change the observed associations, but the 95 % CI became wider. The results in subgroups from analyses stratified by age or BMI at enrolment were not systematically different. In conclusion, the present study suggests that fish consumption has no appreciable association with body-weight gain.<br/>
        </p><p>PMID: 22716915 [PubMed - indexed for MEDLINE]</p>
    ]]></description>
    <author> Jakobsen MU, Dethlefsen C, Due KM, May AM, Romaguera D, Vergnaud AC, Norat T, Sørensen TI, Halkjær J, Tjønneland A, Boutron-Ruault MC, Clavel-Chapelon F, Fagherazzi G, Teucher B, Kühn T, Bergmann MM, Boeing H, Naska A, Orfanos P, Trichopoulou A, Palli D, Santucci De Magistris M, Sieri S, Bueno-de-Mesquita HB, van der A DL, Engeset D, Hjartåker A, Rodríguez L, Agudo A, Molina-Montes E, Huerta JM, Barricarte A, Amiano P, Manjer J, Wirfält E, Hallmans G, Johansson I, Khaw KT, Wareham NJ, Key TJ, Chajès V, Slimani N, Riboli E, Peeters PH, Overvad K</author>
    <category>Br J Nutr</category>
    <guid isPermaLink="false">PubMed:22716915</guid>
</item>

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